Allergic rhinitis: impact, diagnosis, treatment and management

pharmaceutical-journal.com/research/review-article/allergic-rhinitis-impact-diagnosis-treatment-and-
management/20201509.article
Clinical Pharmacist 9 AUG 2016 By Diana S Church , Martin K Church , Glenis K Scadding

Abstract
Allergic rhinitis results from an immunological abnormality in which atopic individuals
produce immunoglobulin E (IgE) to allergens (e.g. pollen, house dust mites, animal dander
and moulds). IgE activates mast cells, which respond by releasing inflammatory mediators.
Histamine stimulates the early symptoms, predominately mucus production, nasal itching
and sneezing. Leukotrienes and cytokines attract and activate eosinophils to cause allergic
inflammation, which is primarily responsible for nasal blockage. When untreated, these
symptoms can potentially impair patients’ ability to sleep and perform optimally in their
daily professional or personal life. Children’s education is also particularly affected by
untreated symptoms. Treatment is primarily with second generation H 1 -antihistamines,
which are particularly effective against the early symptoms, and intranasal corticosteroids,
which reduce allergic inflammation and improve nasal blockage. First generation H1 -
antihistamines should be avoided because they exacerbate the psychogenic effects of allergic
rhinitis. This review article aims to provide pharmacists and other healthcare professionals
with an understanding of the impact of undiagnosed allergic rhinitis and how to diagnose
and treat it effectively.
Keywords: allergy, allergens, allergic rhinitis, antihistamine, corticosteroids, histamine,
immunology, inflammation, pollen.
Original submitted: 10 June 2016; Revised submitted: 29 June 2016; Accepted for
publication: 04 July 2016; Published online: 09 August 2016

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 Source: CNRI / Science Photo Library
Caused by an allergy to pollen, this inflamed mucosa shows its ciliated (hairy) surface overgrown in patches.
Cilia are common on the epithelium of the respiratory tract, where their beating serves to remove particles of
dust, pollen, and other foreign material. Here, an allergy to pollen has resulted in the cilia lengthening.

Key points:
Allergic rhinitis occurs in atopic individuals who produce IgE to allergens, such
as pollen, house dust mites, animal dander and moulds.
Histamine stimulates the early symptoms, predominately mucus production,
nasal itching and sneezing. This may respond well to non-sedating H1 -
antihistamines.
Subsequent allergic inflammation gives rise to nasal blockage. This responds to
nasal steroids.
When untreated, allergic rhinitis can potentially impair patients’ ability to sleep
and perform optimally in their daily professional or personal life. Children’s
education is also particularly affected.
First generation H1 -antihistamines should be avoided because they
exacerbate the psychogenic effects of allergic rhinitis.

Introduction
Allergic rhinitis is a common allergic disease with increasing prevalence; recent
estimates suggest it affects over 30% of individuals, particularly, but not exclusively,
teenagers and young adults[1],[2]. While considered by many as a trivial disease, allergic
rhinitis, in addition to the nasal and ocular symptoms, is crucially linked to impairments
in information processing and changes in attention-related cognitive processes[3].
However, it has been estimated that up to 90% of allergic rhinitis patients are
untreated, insufficiently treated or inappropriately treated[4]. This has the potential to
impair patients’ ability to perform optimally in their daily professional and personal life.

Pathological and psychological effects of untreated allergic rhinitis

Allergic rhinitis generally develops during childhood and it is the most common chronic
allergic disorder seen in children[5]. Studies have shown that these children can
experience significant impairment through multiple physical and psychological aspects.
Their symptoms, particularly a runny nose, mean that children are often embarrassed
in school, have decreased social interaction and are at double the risk of accidental
injury[5],[6]. Nasal congestion, in particular, is associated with sleep disturbance and
resultant daytime fatigue[7]. Two studies have concluded that untreated allergic rhinitis
has a marked detrimental effect on children’s learning and examination
performance[8],[9]. This is particularly important considering that a quarter of UK
school-age children suffer with allergic rhinitis[10], most of whom will have their peak
symptoms in spring and summer, which can coincide with important school
examinations. The correlation between allergic rhinitis and negative effects on learning
should be an area of concern for all professionals involved in their care.

The overall quality of life reduction resulting from allergic rhinitis in adults is well 2/16
The overall quality of life reduction resulting from allergic rhinitis in adults is well
established – it has a detrimental effect on adult cognitive processes (e.g. productivity
at work), as well as other common attention-requiring activities, such as
driving[4],[11],[12]. In a study assessing the effect of nasal allergen provocation of
seasonal allergic patients on driving performance, it was demonstrated that
symptomatic and untreated patients had significantly impaired driving ability, the
magnitude of which was comparable to having a blood alcohol level of 0.05%, the legal
limit in many countries[13]. In addition to acute symptoms, sleep disturbances may
exacerbate impairment of psychomotor performance, including driving[14],[15],[16],[17].
Patients with allergic rhinitis are often affected by physical conditions (e.g. otitis media,
eustachian tube dysfunction, sinusitis[18]) and other allergic conditions (e.g. asthma
and eczema[19]). Therefore, allergic rhinitis is an illness that affects multiple aspects of
patient’s life[19], can be a source of multiple doctor appointments and has complex
effects on society as a whole. Therefore, optimal management of the disease should
address both its physical and mental consequences.

Mechanisms of allergic rhinitis

The roots of allergy are in parasitology, when a nematode parasite attacking the nasal
mucosa. On first presentation, the immune system is stimulated to produce
immunoglobulin E (IgE) that will bind to and prime mast cells and other inflammatory
cells. On a subsequent presentation, nematode antigens interact with the mast cell IgE,
causing it to release preformed histamine to make the local environment hostile (e.g.
producing mucus and stimulating sensory nerves to cause sneezing). Mast cells also
produce cytokines to stimulate the influx inflammatory cells, particularly eosinophils
that contain several toxic proteins with which they kill the nematode and cause local
inflammation. Patients with allergies mount the same response to allergens as
nematode antigens[20],[21]. The series of early immune system events in patients with
allergic rhinitis is presented in Figure 1.

Figure 1: Immune system events in patients with allergic rhinitis

Panel A demonstrates early immune system events, while panel B shows the later inflammatory allergic
response that increases the severity and persistence of the initial symptoms in patients with allergic rhinitis.
See text for an explanation of the events (numbered).

Panel A demonstrates (1) allergens (e.g. pollen, house dust mites, animal dander and 3/16
Panel A demonstrates (1) allergens (e.g. pollen, house dust mites, animal dander and
moulds) penetrating the nasal epithelium. (2) Allergen interacts with IgE, shown in red,
to activate the mast cell. (3) Histamine is the primary mediator released in this early
phase of the response. It has three immediate main effects: (4) stimulation of mucosal
goblet cells to produce watery mucus; (5) stimulation of sensory nerves to cause nasal

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itching and sneezing; and (6) vasodilation and tissue oedema, which contribute to nasal
blockage. These effects are primarily histamine-mediated so antihistamines are
effective in relieving these symptoms.
Panel B shows the later inflammatory allergic response that increases the severity and
persistence of the initial symptoms, resulting in a chronic phase of allergic rhinitis.
Mast cell activation also produces cytokines, responsible for the attraction of more
mast cells and the influx and activation of other inflammatory cells, particularly
eosinophils (7)[22]. Eosinophils contain aggressive proteinaceous mediators (8) that
stimulate sensory neurones to dramatically increase the production and release of
neuropeptides (9). These neuropeptides act on special venous capacitance vessels (10)
present in the nasal turbinates, causing dilatation and reduced emptying. This is the
primary cause of nasal blockage.

Mechanisms of ocular symptoms

Patients with allergic rhinitis may also experience ocular symptoms, primarily
reddened, itchy and watery eyes. Classically these symptoms were believed to be
caused by the allergen landing on the conjunctival lining of the eye, with subsequent
activation of the conjunctival mast cells[23]. It is now believed that these symptoms are
partly the result of a naso-ocular reflex in which allergic inflammation in the nose
stimulates the trigeminal nerve with subsequent release of neuropeptides in the
tears[24]. These neuropeptides activate conjunctival mast cells that release histamine
but cause little subsequent eosinophil infiltration and allergic inflammation[23]. During
periods of high atmospheric levels, pollen impaction on the conjunctiva may induce a
more severe form of vernal conjunctivitis in which eosinophil infiltration stimulated
allergic inflammation[25]. If a severe form of vernal conjunctivitis is suspected, the
patient should be referred to their GP.

Diagnosis of allergic rhinitis by pharmacists

Historically, diagnosis of allergic rhinitis has been made by primary healthcare
practitioners. However, pharmacists are now being encouraged to make the primary
diagnosis of allergic rhinitis and establish a management and therapy plan[26].
Although it should be emphasised that complex cases, or cases where there may by an
alternative diagnosis, should always be referred to a GP.
Allergic rhinitis symptoms, including runny nose, itching, sneezing and nasal blockage,
are similar to those of the common cold and can be present intermittently, giving the
false suggestion of recurrent ‘colds’[27]. This is more common in patients who are
allergic to pollens or outdoor moulds (rather than pets or house dust mites), which are
released into the air and cause symptoms during specific periods of time throughout
the year (see ‘Figure 2: Seasonal considerations’).

Taking a history from the patient

When questioning the patient, pharmacists should listen for indicators that can lead to
the diagnosis of allergic rhinitis, for example:
recurrence at a particular time of year or day, or variability of symptoms,
suggesting worsening on exposure to the relevant allergen;
involvement of the eyes (itching, watering, redness, puffiness); or
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 predominance of itch as a symptom, which can also involve the pharynx and ears.
Allergic rhinitis is more likely if there is a past or family history of allergic disease,
but can also occur as the first manifestation of allergy in a previously unaffected
person.

When taking the patient’s history, it is important to be aware that they might not often
offer all the clues for diagnosis, so pharmacists may have to ask specific questions to
find out more information. For example, a patient with allergy to house dust mites or
animals may complain of sneezing, having a runny nose and blocked nose in the past
one or two weeks, but they might not realise until asked that their nose has been
blocked to a less severe degree for a much longer time. The pharmacist should also
enquire about new allergens in the home, work, or school environment, as well as
symptoms of asthma (shortness of breath accompanied by wheeze, reduced exercise
tolerance or nocturnal symptoms), which often accompany poorly controlled allergic
rhinitis.

Seasonal considerations

Patients may be allergic to trees, plants and

Figure 2: The seasons of major plant
allergens and house dust mite
The lines refer to the times of year at which different
allergens peak. Note that house dust mite levels are
highest in the winter when doors and windows are
closed in centrally heated homes.
fungi that use the wind to disperse their pollen
or spores [28]. Higher amounts of pollens are
released during dry, warmer days when the
chance of their satisfactory dispersion is
maximum (see Figure 2). Visually these plants
are unspectacular in contrast to those with
colourful flowers to attract bees and other
insects to cross-pollinate them. Individuals are
rarely allergic to this latter type[28].
While high amounts of pollen and fungal
spores are released during warmer days
compared to colder ones, house dust mite
allergens are present all year round. However,
these tend to be higher indoors during winter
when windows are shut and the humid,
centrally heated atmosphere is optimum for
their reproduction[29].

Further testing

With a clear patient history, diagnosis can be made without further tests. However, if in
doubt, looking for the likely IgE molecules by skin prick or blood test can be helpful,
although this should be guided by history, rather than performed in a random fashion.
Random screening of multiple possible allergens is inadvisable because positive tests
do not always indicate clinical disease; many individuals with allergen-specific IgE do
not develop symptoms[30]. Furthermore, a positive test to an allergen with no
pertinence to patient’s history has no relevance for diagnosis and might result in over-
diagnosis and unnecessary stress for the patient. Testing should always be considered
in the context of the possible clinical benefit, which can be from allergen avoidance, if
the patient is able and willing to comply, or allergen specific immunotherapy.
6/16
Treatment
This section assesses the drugs only briefly – further information and the British
Society for Allergy & Clinical Immunology (BSACI) guidelines for the management of
allergic and non-allergic rhinitis[31] are included in later sections.
H1 -antihistamines are effective in relieving histamine-induced symptoms, including
itch, runny nose and/or sneezing[31]. They have a lesser effect on nasal blockage but
can be effective as a single medicine in patients with mild to moderate forms of allergic
rhinitis [31]. They have a rapid onset of action and can be used as a rescue medicine to
help alleviate the symptoms of the onset of acute allergic rhinitis.
Intranasal corticosteroids are the primary treatment for nasal obstruction[31] and act
by reducing cytokine production thereby reducing eosinophil recruitment. They also
reduce eosinophil activation and mediator release[32].
Leukotriene receptor antagonists (LTRAs) are given as tablets and may be effective
in some patients but not all [33]. They reduce the effects of the leukotriene C4 (LTC4) that
activated mast cells and eosinophils secrete in order to enhance the recruitment of
more eosinophils and thereby reduce allergic inflammation[34]. The LTRAs montelukast
and zafirlukast are available on medical prescription only (POM). Leukotriene synthesis
inhibitors (e.g. zileuton), are not available in the UK.
Nasal decongestants (e.g. xylometazoline and oxymetazoline), are asympathetic
receptor stimulants and cause constriction of the arterial vessels delivering blood to
the nasal capacitance vessels, therefore starving them of blood[35]. They may be given
locally or orally. When given as nasal drops, they are briefly effective and rapidly acting
but they may only be used for short periods – usually four to ten days[31]. Regular use
induces a decrease in the number of a-receptors in the blood vessels rendering a
reduced effectiveness with time (tolerance)[35]. If used for longer periods, rhinitis
medicamentosa, a condition characterised by nasal congestion without rhinorrhoea or
sneezing, may occur because of a reduction of blood vessel a-receptors thus paralysing
the physiological local vasoconstriction process[7]. Patients should be counselled
regarding this process.
Oral decongestants (e.g. pseudoephedrine) are only weakly effective in reducing
nasal obstruction but have a longer duration of up to six hours (with slow release
preparations)[31]. Owing to their sympathomimetic effects, they should not be used by
individuals with high blood pressure or heart problems [36].
Saline douching, although relatively uncommon in UK, is a safe and inexpensive
method of reducing symptoms in children and adults with seasonal rhinitis by washing
out sticky mucus from the nose[31].
The treatment of ocular symptoms of allergic rhinitis is summarised in Box 1.

Box 1: Treatment of ocular symptoms

1. Intranasal corticosteroids are the most effective treatment for reducing
nasal inflammation and, consequently, are effective in improving conjunctival
symptoms[37].
2. H1-antihistamine eye drops have a similar efficacy profile to oral
antihistamines with the advantage of a significantly faster onset of action[38].
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 3. Topical chromones, sodium cromoglycate or nedocromil sodium, which
are available as topical eye preparations, are also weakly effective. Although
purported to be mast cell stabilisers, they most likely affect the inhibition of
sensory nerve activation, thereby reducing itching[39].

Selecting the right treatment

Oral antihistamines are the first-line treatment used by most patients, doctors and
pharmacists for all allergic rhinitis.
When selecting the most appropriate antihistamine to manage allergic rhinitis,
healthcare professionals should be aware of the significant detrimental effect of first
generation antihistamines (FGAH) on cognitive processes in all patient groups[40].
Histamine acting on H1 -receptors in the brain has a completely different function to
that in the periphery. In the brain, it has an arousal effect and aids concentration and
learning[40]. FGAHs (e.g. chlorpheniramine, diphenhydramine, hydroxyzine and
ketotifen) readily penetrate into the central nervous system (CNS) and bind to the H1 -
receptors in the brain, causing drowsiness and poor attention[40].
Studies in children have demonstrated that FGAHs exacerbate the detrimental effect of
allergic rhinitis on learning ability[8]. Furthermore, in teenagers sitting summer mock
GCSE examinations, untreated allergic rhinitis caused a 40% increased likelihood of
students dropping an examination grade. FGAHs increased this to 70%[9].
In adults the detrimental effects of allergic rhinitis on quality of life and productivity at
work are exacerbated by FGAHs, even at the lowest doses recommended by
manufacturers[40]. The effects of FGAHs on the CNS are similar to and additive with
those produced by alcohol or other CNS-sedatives, and bedtime dosing with FGAHs
may have hangover effects the next day due to their long elimination half-life value[40].
Furthermore, FGAHs may significantly reduce driving ability to potentially dangerous
levels[40],[41], particularly in the elderly and those who combine the drug with alcohol
ingestion. One study suggests that 25% of individuals older than 65 years of age have
some cognitive impairment, often with no overt sign of dysfunction[42]. Administration
of FGAHs to this population increases the risk of inattention, disorganised speech,
altered consciousness and impaired function or alertness[43],[44]. In addition, because
of their anticholinergic activity, FGAHs significantly increase the risk for development of
dementia[45].
Therefore, the British and European Guidelines for both allergic rhinitis and urticaria
specify that only second generation antihistamines should be used for symptom relief,
because they penetrate less well into the brain than FGAHs and have negligible
anticholinergic effects[31],[46]. In the UK, cetirizine and loratadine are currently the only
SGAHs available for patients to buy over-the-counter (OTC). There are many others
(including levocetirizine, desloratadine, rupatadine, fexofenadine and bilastine) that are
available as prescription-only medicines (POM). Even though SGAHs are stated to be
minimally sedating, there are some patients who suffer sedation and psychomotor
retardation, especially if other sedatives or alcohol are taken concomitantly[40].
Fexofenadine and bilastine are the least sedating SGAHs currently available because
they are actively pumped out of the blood–brain barrier by p-glycoprotein (a proton
pump)[47]. However, these must be taken on an empty stomach for adequate
absorption.

Intranasal antihistamines are more effective at reducing nasal symptoms than oral 8/16
Intranasal antihistamines are more effective at reducing nasal symptoms than oral
antihistamines, but do not treat extra-nasal symptoms[48]. Azelastine nasal spray is
available OTC.
Although antihistamines demonstrate efficacy, for the control of symptoms like
sneezing, itching and rhinorrhoea or eye streaming, they are considerably less effective
than intranasal corticosteroids that have a much stronger anti-inflammatory effect and
are more effective in treating nasal obstruction[49]. Corticosteroids should be used as
the therapeutic of choice for anything more than mild disease[31].

Intranasal steroids

Intranasal steroids are the most effective treatment for reducing nasal inflammation
and improving conjunctival symptoms[23],[50]. In the UK, beclomethasone dipropionate
and fluticasone propionate are available OTC, while fluticasone furoate and
mometasone furoate are POM.
When bought OTC or even when prescribed by a medical practitioner, nasal steroids
are often wrongly used or not used at all, because of fears of “steroids”. Therefore, it is
important to explain to the patient that the dose of nasal steroids is in microgram
quantities and for most of the common molecules there is minimal systemic
bioavailability (i.e. the amount of active drug reaching the systemic circulation). There
is a variation between molecules, with fluticasone propionate, furoate and
mometasone furoate being the least bioavailable from the nose. It is best to use the
spray in the morning, putting it next to the toothbrush to aid memory. A second dose
can be used in the evening if needed, or if the morning one was forgotten.
The method of application for nasal sprays and drops is shown in Figure 3. Spraying
the nasal septum and sniffing the spray straight back into the throat should be
avoided.

Figure 3: Method of application for nasal sprays and nasal drops

Source: Reproduced from the BSACI allergic rhinitis guidelines with permission.
(a) Correct procedure for the application of nasal sprays. (b) Correct procedure for the installation of nasal
drops.

Begin treatment early and take it daily

It is important to inform patients that nasal steroids do not work immediately. Nasal
steroids have been shown to take at least several days to reach full effectiveness and
maximal effect may not be apparent for two weeks[29].
9/16
For patients with intermittent symptoms (e.g. those allergic to pollens) it has been
demonstrated that if therapy with topical nasal corticosteroids is begun a week or two
before symptoms are expected, symptoms have delayed onset and reduced
severity[51]. Thus, it can be useful to ask patients with known seasonal allergic rhinitis
to make a note of when their symptoms started in the current year so that in the
following year they can start the treatment earlier.
Similarly, both antihistamines and nasal corticosteroids, particularly the latter, are
more effective if used on a daily basis, rather than being stopped and started[51]. The
symptoms for both persistent and intermittent allergic rhinitis are underlined by an
ongoing inflammation that is usually present at subclinical levels, even in the absence
of symptoms[52]. Daily treatment helps to prevent this low-grade ongoing subclinical
allergic inflammation in the nasal lining increasing to a threshold at which symptoms
occur and, thus, reduces the rate and severity of exacerbations[51]. Therefore,
pharmacists should explain to patients that the drug makes them free of symptoms,
rather than curing their disease, so stopping treatment early will result in the
reappearance of symptoms. If they do not get relief from the prescribed medication,
they should seek further advice since other treatment options might be available.
A simple way to keep track of patients’ symptoms is for them to use the MACVIA-ARIA
visual analogue scale, via a mobile phone app[53]. If their total symptom score is over
half way along the line, the treatment needs to be augmented or changed. Switching
from one brand of antihistamine or intranasal corticosteroid to another is not the
answer.
BSACI guidelines suggest that in more severe disease nasal corticosteroids and
antihistamines may be used together[31] and the combination of nasal corticosteroid
plus nasal antihistamine (e.g. azelastine plus fluticasone) has been reported to be more
effective than either alone[54],[55]. However, this drug combination is a POM at present.

Management of allergic rhinitis

The BSACI guidelines provide direction to help healthcare professionals direct therapy
for allergic rhinitis[31]. A simple algorithm for the treatment of allergic rhinitis is shown
in Figure 4.

Figure 4: A simple algorithm for the treatment of allergic rhinitis

Source: This figure is adapted from the BSACI allergic rhinitis guidelines.
The progression of treatment goes from left to right as severity increases.

For patients with intermittent allergic rhinitis caused by seasonal allergens, as the 10/16
For patients with intermittent allergic rhinitis caused by seasonal allergens, as the
season wanes and pollen levels in the atmosphere reduce, treatment can be gradually
reduced, if the symptoms are completely controlled, and stopped once the season is
over.
Patients with persistent allergic rhinitis, such as those allergic to perennial allergens
(e.g. house dust mite, animals or indoor moulds) or those with mixed seasonal and
perennial allergies, need longer term therapy. Once complete control of symptoms has
been achieved, a gradual ‘step down’ can be attempted. The treatment should be
continued for at least three to six months after complete symptom control. If
symptoms recur, the treatment should be restarted, usually for longer periods (e.g. 6–
12 months or even for life). There are some concerns about possible lining atrophy
with long-term use of intranasal steroids. However, in practice, with correct use this
does not occur, probably because of rapid movement by mucocilliary clearance[56].
Spraying the nasal septum repeatedly can result in soreness, epistaxis (nose bleed) and
possibly even perforation, which is why correct technique is important.

Allergen avoidance

Studies involving concomitant multiple strict allergen control measures showed that it
is possible to achieve a significant reduction in allergen exposure and, consequently, in
symptoms[57],[58]. However, in real life situations, avoiding aeroallergens to an extent
where it would make a difference in patients’ symptoms is difficult to reach. With pollen
allergy, closing windows at night, driving with closed windows or wearing wrap-around
glasses outdoors can prevent symptom exacerbation[31]. Avoiding being outside during
thunderstorms can also help reduce symptoms, because the sudden change from a
dry to a wet climate causes pollen grains to rupture and release their allergenic into
smaller particles, which can be easily inhaled into the lower airways and cause attacks
of allergic rhinitis and asthma[59].

Immunotherapy

Allergen-specific immunotherapy is the treatment in which a patient’s immune system

is rendered tolerant to an allergen by giving increasing doses of the allergen in a
controlled fashion[60],[61]. When used correctly, it is the only treatment that can alter
disease course[60]. There is also evidence that it can reduce development of further
sensitisations and progression of allergic rhinitis to asthma, although current trials
require positive outcomes to determine if children with allergic rhinitis, who are likely
to progress to asthma, will benefit from it[61].
Few seasonal allergic rhinitis patients warrant immunotherapy treatment; it should
only be considered when allergic rhinitis is debilitating and poorly controlled by
pharmacotherapy. Special consideration should be given to badly affected young
people who face years of summertime examinations or adults whose functioning is
disturbed (e.g. surgeons who have severe eye symptoms or sneezing bouts)[61].
Immunotherapy is currently available for allergic rhinitis caused by pollen, moulds,
house dust mite and animal allergens.

There are two main routes by which immunotherapy is administered; subcutaneously 11/16
There are two main routes by which immunotherapy is administered; subcutaneously
and sublingually. Subcutaneous immunotherapy involves allergen injections at regular
time intervals in a hospital by trained medical staff. With treatment lasting several
years, patient commitment to attending hospital appointments is essential. Sublingual
immunotherapy is considered to be much safer. The initial dose is given under
supervision, but can then be continued on a daily basis at home[62],[63]. However,
patients should be warned against poor compliance, which is a concern with this form
of immunotherapy[64].

Management in specific patient groups

Children with allergic rhinitis

Children metabolise drugs less well than adults because the liver enzymes mature
slowly and only reach maximal levels at around ten years of age[65]. However, renal
clearance is well developed. Consequently, it is preferable that young children are
prescribed an antihistamine that is not metabolised but excreted unchanged in the
urine[66]. Of the OTC preparations, this means cetirizine is preferable, rather than
loratadine.
A nasal steroid with low systemic bioavailability should be used at the lowest possible
dose to control symptoms, particularly nasal congestion and obstruction. Compliance
and efficacy is improved if the child is taught how to use the nasal spray[31]. In older
children where liver metabolic enzymes are increasing, it may be preferable to use
fluticasone, which is cleared by first metabolism, rather than beclomethasone that is
not and, consequently, may accumulate[67]. Furthermore, fluticasone is available for
children from four years of age, while beclomethasone is only available for children
from six years of age.
Allergic rhinitis in pregnancy
Most medicines cross the placenta, and should only be prescribed when the apparent
benefit is greater than the risk to the foetus[31]. Regular nasal douching may be helpful.
Of the antihistamines, both loratadine and cetirizine are recommended because they
appear to have good safety records because they have been widely used in pregnant
women[68]. Similarly, beclomethasone and fluticasone appear safe. However,
decongestants should be avoided[31]. Local application of chromones, which have not
demonstrated teratogenic effects in animals, are probably the safest drug choice for
use in the first three months of pregnancy because systemic absorption is negligible,
although they require multiple daily administrations[31].

Conclusion
The treatment of allergic rhinitis involves non-sedating H1 -antihistamines to reduce
rhinorrhoea and nasal itching, and corticosteroids to reduce allergic inflammation and
nasal blockage. They should be used on a daily basis rather than on ad hoc when
symptoms are bad. Pharmacists should advise patients about how to correctly
administer their treatment, as well as reviewing its effectiveness regularly. Patients
should be advised of alternative treatment options where appropriate.

Financial and conflicts of interests dislosure:

Martin Church has been a speaker or consultant for Almirall, FAES Pharma, 12/16
 Martin Church has been a speaker or consultant for Almirall, FAES Pharma,
Menarini, Moxie, MSD, Novartis, UCB Pharma, Sanofi-Aventis and Uriach. Glenis
Scadding has had research grants from GSK & ALK and has been a speaker or
consultant for ALK, Astra Zeneca, Brittania Pharmaceuticals, Capnia, Church &
Dwight, Circassia, GSK, Groupo Uriach, Meda, Merck, MSD, Ono Pharmaceuticals,
Oxford Therapeutics, Sanofi-Aventis, UCB. Diana Church has no relevant affiliations
or financial involvement with any organisation or entity with a financial interest in or
financial conflict with the subject matter or materials discussed in the manuscript
apart from those disclosed. No writing assistance was utilised in the production of
this manuscript.

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Citation: Clinical Pharmacist, August 2016, Vol 8, No 8, online | DOI:
10.1211/CP.2016.20201509

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